852 research outputs found

    Shock waves in thermal lensing

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    We review experimental investigation on spatial shock waves formed by the self-defocusing action of a laser beam propagation in a disordered thermal nonlinear media.Comment: 9 pages, 12 figure

    Shock waves in disordered media

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    We experimentally investigate the interplay between spatial shock waves and the degree of disorder during nonlinear optical propagation in a thermal defocusing medium. We characterize the way the shock point is affected by the amount of disorder and scales with wave amplitude. Evidence for the existence of a phase diagram in terms of nonlinearity and amount of randomness is reported. The results are in quantitative agreement with a theoretical approach based on the hydrodynamic approximation.Comment: 4 pages, 5 figure

    Seismic Vulnerability Assessment of a Historical Church: Limit Analysis and Nonlinear Finite Element Analysis

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    The seismic vulnerability of a historical Basilica church located in Italy is studied by means of limit analysis and nonlinear finite element (FE) analysis. Attention is posed to the failure mechanisms involving the façade of the church and its interaction with the lateral walls. In particular, the limit analysis and the nonlinear FE analysis provide an estimate of the load collapse multiplier of the failure mechanisms. Results obtained from both approaches are in agreement and can support the selection of possible retrofitting measures to decrease the vulnerability of the church under seismic loads

    Nonlinear Gamow vectors in nonlocal optical propagation

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    Shock waves dominate in a wide variety of fields in physics dealing with nonlinear phenomena, nevertheless the description of their evolution is not resolved for the entire dynamics. Here we propose an analytical method based on Gamow vectors, which belong to irreversible quantum mechanics. We theoretically and experimentally show the appearance of these decaying states during shock evolution allowing to describe the whole wave propagation. These results open new ways to the control of extreme nonlinear regimes such as supercontinuum generation or in the analogies of fundamental physical theories

    The european flood alert system EFAS – Part 2: Statistical skill assessment of probabilistic and deterministic operational forecasts

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    Since 2005 the European Flood Alert System (EFAS) has been producing probabilistic hydrological forecasts in pre-operational mode at the Joint Research Centre (JRC) of the European Commission. EFAS aims at increasing preparedness for floods in trans-national European river basins by providing medium-range deterministic and probabilistic flood forecasting information, from 3 to 10 days in advance, to national hydro-meteorological services. <br><br> This paper is Part 2 of a study presenting the development and skill assessment of EFAS. In Part 1, the scientific approach adopted in the development of the system has been presented, as well as its basic principles and forecast products. In the present article, two years of existing operational EFAS forecasts are statistically assessed and the skill of EFAS forecasts is analysed with several skill scores. The analysis is based on the comparison of threshold exceedances between proxy-observed and forecasted discharges. Skill is assessed both with and without taking into account the persistence of the forecasted signal during consecutive forecasts. <br><br> Skill assessment approaches are mostly adopted from meteorology and the analysis also compares probabilistic and deterministic aspects of EFAS. Furthermore, the utility of different skill scores is discussed and their strengths and shortcomings illustrated. The analysis shows the benefit of incorporating past forecasts in the probability analysis, for medium-range forecasts, which effectively increases the skill of the forecasts

    The secondary KIT mutation p.Ala510Val in a cutaneous mast cell tumour carrying the activating mutation p.Asn508Ile confers resistance to masitinib in dogs

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    Background: Gain-of-function mutations in KIT are driver events of oncogenesis in mast cell tumours (MCTs) affecting companion animals. Somatic mutations of KIT determine the constitutive activation of the tyrosine kinase receptor leading to a worse prognosis and a shorter survival time than MCTs harbouring wild-type KIT. However, canine MCTs carrying KIT somatic mutations generally respond well to tyrosine kinase inhibitors; hence their presence represents a predictor of treatment effectiveness, and its detection allows implementing a stratified medical approach. Despite this, veterinary oncologists experience treatment failures, even with targeted therapies whose cause cannot be elucidated. The first case of an MCT-affected dog caused by a secondary mutation in the tyrosine kinase domain responsible for resistance has recently been reported. The knowledge of this and all the other mutations responsible for resistance would allow the effective bedside implementation of a deeply stratified and more effective medical approach. Case presentation: The second case of a canine MCT carrying a different resistance mutation is herein described. The case was characterised by aggressive behaviour and early metastasis unresponsive to both vinblastine- and masitinib-based treatments. Molecular profiling of the tumoural masses revealed two different mutations; other than the already known activating mutation p.Asn508Ile in KIT exon 9, which is tyrosine kinase inhibitor-sensitive, a nearly adjacent secondary missense mutation, p.Ala510Val, which had never before been described, was detected. In vitro transfection experiments showed that the secondary mutation did not cause the constitutive activation by itself but played a role in conferring resistance to masitinib. Conclusions: This study highlighted the importance of the accurate molecular profiling of an MCT in order to improve understanding of the molecular mechanism underlying tumourigenesis and reveal chemoresistance in MCTs for more effective therapies. The detection of the somatic mutations responsible for resistance should be included in the molecular screening of MCTs, and a systematic analysis of all the cases characterised by unexpected refractoriness to therapies should be investigated in depth at both the genetic and the phenotypic level

    A large deletion in the GP9 gene in Cocker Spaniel dogs with Bernard-Soulier syndrome

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    Inherited bleeding disorders including abnormalities of platelet number and function rarely occur in a variety of dog breeds, but are probably underdiagnosed. Genetically characterized canine forms of platelet disorders provide valuable large animal models for understanding similar platelet disorders in people. Breed-specific disease associated genetic variants in only eight different genes are known to cause intrinsic platelet disorders in dogs. However, the causative genetic variant in many dog breeds has until now remained unknown. Four cases of a mild to severe bleeding disorder in Cocker Spaniel dogs are herein presented. The affected dogs showed a platelet adhesion defect characterized by macrothrombocytopenia with variable platelet counts resembling human Bernard-Soulier syndrome (BSS). Furthermore, the lack of functional GPIb-IX-V was demonstrated by immunocytochemistry. Whole genome sequencing of one affected dog and visual inspection of the candidate genes identified a deletion in the glycoprotein IX platelet (GP9) gene. The GP9 gene encodes a subunit of a platelet surface membrane glycoprotein complex; this functions as a receptor for von Willebrand factor, which initiates the maintenance of hemostasis after injury. Variants in human GP9 are associated with Bernard-Soulier syndrome, type C. The deletion spanned 2460 bp, and included a significant part of the single coding exon of the canine GP9 gene on dog chromosome 20. The variant results in a frameshift and premature stop codon which is predicted to truncate almost two-thirds of the encoded protein. PCR-based genotyping confirmed recessive inheritance. The homozygous variant genotype seen in affected dogs did not occur in 98 control Cocker Spaniels. Thus, it was concluded that the structural variant identified in the GP9 gene was most likely causative for the BSS-phenotype in the dogs examined. These findings provide the first large animal GP9 model for this group of inherited platelet disorders and greatly facilitate the diagnosis and identification of affected and/or normal carriers in Cocker Spaniels
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